Neuropathy "The Painful Enigma"

Inflammation is the human body’s natural response to injury, infection, or illness. However, too much inflammation can affect your overall health and wellness, especially when you have inflammation in the brain. Brain inflammation can even affect your mental and emotional well-being. Understanding the causes and symptoms of inflammation in the brain can help determine the best treatment option. Dr. Santosh Kesari describes that brain inflammation can be due to various reasons, including toxins like tobacco or alcohol, diabetes, hypertension, infections, trauma, aging, diet, and stress.

“Some inflammation is acute, short-lasting, and possibly reversible but other types of inflammation are chronic and continue to cause brain damage,” Dr. Kesari states. “These may be cumulative and not readily reversible, such as Alzheimer’s disease.” With an overactive immune system, such as in people who have multiple sclerosis or encephalitis which is inflammation in the brain, several people may already be genetically predisposed to experience brain inflammation. Severe inflammation can lead to a variety of symptoms, it may also result in coma, brain damage, or death. The following 7 signs and symptoms may indicate inflammation in the brain. Make sure to seek immediate medical attention if brain inflammation is suspected.

There is plenty of controversies associated with MSG. Researchers believe that the excess consumption of monosodium glutamate can cause asthma, headaches, and even brain health issues. On the other hand, the majority of official sources, including the FDA, claim that MSG is a safe food ingredient. The following article discusses what is monosodium glutamate, or MSG, and its effects on overall health and wellness, exploring both sides of the argument on the food ingredient.  

What is Monosodium Glutamate (MSG)?

MSG is known as monosodium glutamate. It is a common food ingredient that is utilized to enhance flavor in foods. MSG comes from the amino acid, glutamate or glutamic acid, which is one of the most common amino acids found in nature. Glutamate is a non-essential amino acid, which ultimately means that the human body can naturally produce it. Monosodium glutamate also serves a variety of functions in the human body and it is commonly found in almost all types of foods.  

MSG is a white crystalline powder that looks similar to sugar or table salt. It is also made up of a combination of sodium and glutamic acid, known as sodium salt. The glutamic acid in MSG is created by fermenting starches, however, there is no chemical difference between the glutamic acid in monosodium glutamate and that found in natural foods. The glutamic acid in MSG can be easier to absorb because it isn’t bound inside big protein molecules which the body breaks down.  

When compared to other central nervous system (CNS) health issues, chronic neurodegenerative diseases can be far more complicated. Foremostly, because the compromised mitochondrial function has been demonstrated in many neurodegenerative diseases, the resulting problems in energy sources are not as severe as the energy collapse in ischemic stroke. Therefore, if excitotoxicity contributes to neurodegeneration, a different time of chronic excitotoxicity needs to be assumed. In the following article, we will outline what is known about the pathways that may cause excitotoxicity in neurodegenerative diseases. We will specifically discuss that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies.  

When compared to other central nervous system (CNS) health issues, chronic neurodegenerative diseases can be far more complicated. Foremostly, because the compromised mitochondrial function has been demonstrated in many neurodegenerative diseases, the resulting problems in energy sources are not as severe as the energy collapse in ischemic stroke. Therefore, if excitotoxicity contributes to neurodegeneration, a different time of chronic excitotoxicity needs to be assumed. In the following article, we will outline what is known about the pathways that may cause excitotoxicity in neurodegenerative diseases. We will specifically discuss that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies.

Excitotoxicity is characterized as an acute insult which causes nerve cell death due to the excessive activation of iGluRs. Acute excitotoxicity plays a fundamental role in a variety of central nervous system (CNS) health issues, including cerebral ischemia, TBI, and status epilepticus. The mechanisms for acute excitotoxicity are different for every health issue.  

With brain ischemia, L-glutamate-associated and L-aspartate-associated excitotoxicity happen within minutes due to the growth in extracellular cerebral L-glutamate as well as L-aspartate. Because these are also energy-dependent, the abrupt loss of energy due to the shut down of blood flow can ultimately breakdown the neuronal and astroglial membrane. In neurons, membrane depolarization contributes to vesicular discharge. Additionally, energy degradation may even cause a change in their action, therefore, causing L-glutamate and L-aspartate to activate and affect ionic homeostasis which can interrupt EAAT action. The activation of L-glutamate/L-aspartate contributes to excitotoxicity through the over-activation of iGluRs of the NMDA type as demonstrated by the efficiency of NMDA antagonists in animal models of transient cerebral ischemia.  

In TBI, the mechanical tissue damage and the disruption of the blood-brain barrier can trigger acute secondary neurodegeneration, which, together with neuroinflammation and oxidative stress, is associated with L-glutamate activation from intracellular compartments and, therefore, by acute excitotoxicity. Moveover, acute application of the NMDA antagonist MK801 following TBI ameliorates neuronal loss and long-term behavioral abnormalities, among others.  

In status epilepticus, continuing the synchronized activity of excitatory neuronal networks as well as the continuous breakdown of restricting mechanisms is the main source of L-glutamate and L-aspartate activation. As the severity of synchronous activity depends upon the involvement of nerve cells into a neuronal system as well as the capability of a neural cell to withstand excess glutamate mainly depends on the expression pattern of iGluRs, a somewhat restricted and maturation-associated degeneration of neuronal populations which is ultimately caused by prolonged epileptic seizures. The significance of excitotoxicity in status epilepticus is shown as NMDA antagonists, such as ketamine, decrease adrenal loss.

The term excitotoxicity was first employed to demonstrate the capability of L-glutamate, in addition to structurally-associated amino acids, to destroy nerve cells, a process which has been suggested to occur in acute and chronic health issues of the central nervous system (CNS). Excitotoxicity is caused by the excess stimulation of iGluRs into a characteristic loss of cell bodies and dendrites as well as post-synaptic structures. There is a substantial degree of variation in the sensitivity of nerve cells compared to the variety of iGluRs which is associated with the specific receptors demonstrated on the nerve cells and their metabolisms. The susceptibility of neurons to excitotoxicity can be affected with age.  

Acute excitotoxic nerve cell death is believed to occur in reaction to a number of severe insults, including cerebral ischemia, traumatic brain injury (TBI), hypoglycemia, and status epilepticus. However, what about neurodegenerative diseases, such as Alzheimer’s disease? Does chronic excitotoxicity also occur? Could exposure of nerve cells to low but above-average concentrations of L-glutamate, or even glutamatergic neurotransmission through a variety of molecules be involved as previously mentioned, within an extended time period also significantly result in neural cell death? The purpose of the article below is to demonstrate the concepts of acute and chronic glutamate toxicity on the health and wellness of the brain.  

For people who love drinking diet sodas, recent research studies have found that diet drinks can increase the risk of stroke and dementia. Although diet drinks have been previously advertised as a much more healthier, low-calorie alternative than regular carbonated drinks, a closer look at the results of these recent research studies ultimately suggests otherwise.

One research study, consisting of 2,888 participants, ages 45 and older, in the Framingham Heart Study, asked for diet entries to be filled out up to three times within a seven-year period. According to the research study, participants who said they drank one diet soda a day were roughly twice as likely to have a stroke within the next decade than individuals who didn’t drink diet soda. Drinking regular, sugar-sweetened carbonated drinks did not seem to increase the risk of stroke.

However, these types of research studies have only been able to prove an association between diet drinks, stroke and dementia. “Also, only 97 people (about 3 percent) had strokes during the follow-up, which means that only two or even three of those strokes may be associated to drinking diet soda,” stated Dr. Kathryn Rexrode, an associate professor of medicine at Harvard-affiliated Brigham and Women’s Hospital which co-authored a research study on soda intake and stroke risk.

The most common causes of TBI which result in ER visits include slip-and-fall accidents, blows to the head, and automobile accidents. Abrupt forces which jolt the brain violently within the skull, such as shock waves from explosions, which can also cause TBI. Traumatic brain injury can also result from bullet wounds or other injuries which penetrate the skull and brain.

Doctors characterize traumatic brain injury as mild, moderate, or severe depending on whether the injury causes unconsciousness, how long it lasts, and other symptoms. Although most traumatic brain injuries are characterized as mild because they’re not considered life-threatening, even a mild TBI can have serious and long-lasting effects if left untreated.  

Resulting from an impact to the head which interrupts brain function, TBI is a threat to cognitive health in two ways:  

• The effects of traumatic brain injury, which may be long-lasting or even permanent, can include unconsciousness, inability to recall the event, confusion, difficulty learning new information, trouble speaking, unsteadiness, lack of coordination, and health issues associated with vision or hearing, among other common symptoms.
• TBI may increase the risk of developing Alzheimer’s disease or dementia, years after the injury takes place.

According to the Centers for Disease Control and Prevention (CDC), approximately 2.8 million TBI-associated ER visits, hospitalizations, and deaths occurred in 2013, the latest year for which information is available. The purpose of the following article is to discuss traumatic brain injury (TBI) and its connection with Alzheimer’s disease and other health issues.  

Traumatic brain injury (TBI) is one of the most common causes of disability and death in people. About 1.6 million individuals suffer traumatic brain injuries in the United States every year. TBI can cause a process of injury which may ultimately cause a variety of neurodegenerative diseases and other health issues. Many of the neurodegenerative diseases following TBI include health issues such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS).

The mechanisms underlying the pathogenesis which result in these type of neurodegenerative diseases, however, are still completely misunderstood. Where many of the health issues following TBI have a high incidence, there are currently only several treatment approaches which can help prevent the pathological development of chronic neurological diseases.

An understanding of the mechanisms underlying TBI and neurodegenerative diseases is fundamental to determine the possible connection between these health issues, to allow the safe and effective diagnosis and treatment. In the following article, we discuss the pathological mechanisms of neurodegenerative diseases and how they’re associated with traumatic brain injury (TBI), including Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS).

Alzheimer’s disease (AD) is one of the most common types of dementia among older adults. Research studies have demonstrated that pathological changes in the human brain, whether directly or indirectly, can ultimately cause loss of synaptic function, mitochondrial damage, microglial cell activation, and neuronal cell death. However, the pathogenesis of AD is not yet fully understood and there is currently no definitive treatment for the neurological disease. Research studies have demonstrated that the activation and priming of microglial cells may contribute to the pathogenesis of AD.

A proinflammatory status of the central nervous system (CNS) can also cause changes in the function of the microglial cells or microglia. Neuroinflammation is closely associated with the activation of microglia and astrocytes which are connected to a variety of neurological diseases by the synthesis and secretion of inflammatory mediators such as iNOS, ROS, and proinflammatory cytokines. According to research studies, microglial priming is also caused by the inflammation of the CNS.

Therefore, whether microglial priming is the result or the cause of neuroinflammation is still controversial. Microglial cell activation commonly causes an increase of Aβ and tau proteins as well as a decrease of neurotrophic factors, ultimately leading to the loss of healthy brain cells or neurons and the development of neuritic plaques and neurofibrillary tangles which are closely associated with AD. With the progression of Alzheimer’s disease, changes from neuronal dysfunctions which may have no obvious symptoms to memory loss and cognitive impairment may become more noticeable.

Low-level laser therapy (LLLT), also known as photobiomodulation, is the use of low-power lasers or light-emitting diodes (LEDs) for treatment purposes. When LLLT is used on the brain, it is known as transcranial LLLT or transcranial photobiomodulation. Many research studies have shown that LLLT can help treat a variety of brain health issues.  

Different from high-intensity surgical lasers, low-powered lasers do not cut or burn tissue. Instead, these lasers stimulate a biological reaction and promote cells to function properly. Moreover, it’s also easy to use LLLT utilizing red and near-infrared light on your own home. In the article below, we will discuss the brain health benefits of low-level laser therapy (LLLT).  

Inflammatory reactions in the central nervous system (CNS) are currently known to be associated with many neurological disorders. In neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), there is considerable penetration of different leukocyte subsets into the CNS or there is severe activation of microglial cells which increases many inflammatory mediators in the CNS. In acute CNS disorders, including delayed corrosion associated with vasospasm after subarachnoid hemorrhage (SAH), ischemic stroke, spontaneous intracerebral hemorrhage (ICH), and traumatic brain injury (TBI), current evidence from a variety of research studies reveal that inflammation may be a possible target for treatment. Inflammation is becoming a promising region of research study for new treatments.

To speed up the process of translating this information to clinical applications, a number of significant problems have to be addressed as their capacity to continuously identify characteristic cerebral deficits in people with neurodegenerative diseases, the connections of brain injuries to clinical symptoms and genetic diagnosis as well as the level to which the harm respond to various treatment approaches. In this article, findings that address some of these problems are reported by several researchers.

MSG is a food additive which is found in the majority of the industrial foods. It boosts the taste of the food hence attracting customers. There is no value in terms of nutrition and it really does nothing to the eater, however, it can have many effects on foods. MSG is known as an “excitotoxin” or neurotoxin. Research studies have found that it has devastating and degenerative effects on the brain and the nervous system. The neurons or brain cells overstimulate and fatigue to their death. MSG enters the brain through the membranes in the mouth and the throat. It also enters the blood-stream through the digestion of food in the gastrointestinal (GI) tract. MSG “tricks” the human body into believing that it is getting value from these foods.

MSG is not a natural substance found in nature. It’s a man-made chemical from glutamic acid, an amino acid found in proteins. Amino acids do happen naturally in animal cells and in several plant cells. The kinds of amino acids have been processed through the change of this pure form of glutamate. Some of the materials used for this purpose include starches, molasses, and corn. The manipulation procedure generates this type of glutamate. The d-glutamate is not found naturally. The free glutamates can enter the body about eight to ten times faster compared to natural glutamates. Natural glutamate is found in foods such as tomatoes, mushrooms, and milk. Techniques used to manufacture glutamate were not in use before the 1960s. The MSG in use now is not natural. In the article, we will discuss how MSG is associated with neurological diseases.

Many patients with peripheral neuropathy often believe that their painful symptoms are irreversible or permanent. However, Dr. John Coppola and Dr. Valerie Monteiro describe that peripheral neuropathy can be treated by treating the underlying source of the painful symptoms. Several patients discuss their painful peripheral neuropathy symptoms and how these affected their overall quality of life.

Moreover, the patients also discuss how Dr. John Coppola and Dr. Valerie Monteiro helped treat their painful peripheral neuropathy symptoms through the use of a variety of treatment methods and techniques. Dr. Alex Jimenez, doctor of chiropractic in El Paso, TX, can help treat painful symptoms associated with peripheral neuropathy. Dr. Alex Jimenez is the non-surgical choice for chiropractic care and peripheral neuropathy treatment.

Peripheral Neuropathy Recovery Success Stories | El Paso, TX (2019)

Neuropathy is a medical term used to describe a collection of general diseases or malfunctions which affect the nerves.

The causes of neuropathy, or nerve damage, can vary among individuals and these may be caused by different:

• Diseases
• Injuries
• Infections
• Vitamin deficiencies

Neuropathy can also be classified according to the location of the nerves being affected and according to the disease-causing it.

Neuropathy caused by diabetes is called diabetic neuropathy.

Furthermore, depending on which nerves are affected will depend on the symptoms that will manifest.

Peripheral neuropathy is simply referred to as neuropathy, which is a state that happens when the nerves become damaged or injured, oftentimes simply disturbed.

It’s estimated that neuropathy affects roughly 2.4 percent of the general populace and approximately 8 percent of people older than age 55.

Type

Neuropathy can affect any of the three types of peripheral nerves:

• Sensory nerves transmit messages from sensory organs:
• Eyes
• Nose
• Brain
• Motor nerves track the movement of the muscles
• Autonomic nerves regulate the involuntary body functions

Sometimes, neuropathy will only impact one nerve. This is medically referred to as mononeuropathy and instances of it include:

• Ulnar neuropathy affects the elbow
• Radial neuropathy affects the arms
• Peroneal neuropathy affects the knees
• Femoral neuropathy affects the thighs
• Cervical neuropathy affects the neck

Sometimes, two or more isolated nerves in separate regions of the body can become damaged, injured or disrupted, resulting in mono neuritis multiplex neuropathy.

Most of the time, multiple peripheral nerves malfunction at the same time, a condition called polyneuropathy.

Cause

Neuropathies are often inherited from birth or they develop later in life.

The most frequent inherited neuropathy is the Charcot-Marie-Tooth disease, which affects 1 in 2,500 people in the USA.

Although healthcare professionals are sometimes not able to pinpoint the exact reason for an acquired neuropathy, medically referred to as idiopathic neuropathy.

There are many known causes for them, including:

• Systemic diseases - a systemic disease is one that affects the whole body.
• Physical trauma
• Infectious diseases
• Autoimmune disorders

The most frequent systemic cause behind peripheral neuropathy is diabetes, which can lead to chronically high blood glucose levels that harm nerves.

 Other systemic issues can cause neuropathy, including:

1. Kidney disorders permit high levels of nerve-damaging toxic chemicals to flow in the blood
2. Toxins from exposure to heavy metals include:

• Arsenic
• Lead
• Mercury
• Thallium

1. Drugs/medications, including anti-cancer medications, anticonvulsants, antivirals, and antibiotics
2. Chemical imbalances because of liver illnesses.
3. Hormonal diseases, like hyperthyroidism, which disturbs metabolic processes, and potentially induces cells and body parts to exert pressure on the nerves.
4. Deficiencies in vitamins, such as E, B1 (thiamine), B6 (pyridoxine), B12, and niacin can be vital for healthy nerves.
5. Alcohol abuse induces vitamin deficiencies and could harm nerves.
6. Cancers and tumors can exert damaging pressure on nerve fibers and paths.
7. Chronic inflammation can damage protective tissues around nerves, which makes them more vulnerable to compression, getting inflamed and swollen.
8. Blood diseases and blood vessel damage, which may damage or injure nerve tissue by decreasing the available oxygen supply

Symptoms

Depending on the reason and unique to each patient, signs, and symptoms of neuropathy can include:

• Pain
• Tingling
• Burning/prickling sensations
• Increased sensitivity to touch
• Muscle weakness
• Temporary or permanent numbness;
• Paralysis
• Dysfunction in glands or organs
• Impairment in urination and
• Sexual function

Symptoms are dependent on autonomic, sensory, or motor nerves or a combination are affected.

Autonomic nerve damage can start a chain reaction of physiological functions like blood pressure or create gastrointestinal problems and issues.

Damage or dysfunction in the sensory nerves may impact sensations and sense of equilibrium or balance, while injury to motor nerves affects movement and reflexes.

When both sensory and motor nerves are involved, the condition is known as sensorimotor polyneuropathy.

Complications

Peripheral neuropathy may result in several complications, as a result of disease or its symptoms.

Numbness from the ailment can allow you to be less vulnerable to temperatures and pain, making you more likely to suffer from burns and serious wounds.

The lack of sensations in the feet, for instance, can make you more prone to developing infections from minor traumatic accidents, particularly for diabetics, who heal more slowly than other people, including foot ulcers and gangrene.

Furthermore, muscle atrophy may cause you to develop particular physical disfigurements, such as pes cavus, a condition marked by an abnormally high foot arch, and claw-like deformities in the feet and palms.

Treatment

The first step in neuropathy treatment should be finding the root cause that's causing the neuropathy.

Treatment of diseases such as:

• Diabetes
• Guillain-Barre syndrome
• Rheumatoid arthritis
• Sarcoidosis
• Other underlying diseases

Prevents continued nerve damage and in cases heals the damaged nerves.

If you are unaware of any underlying disease that is causing the peripheral neuropathy, make sure to let your doctor know of abnormal symptoms. 

Medication

Peripheral neuropathy can be treated with various medications.

The first type used to treat mild symptoms are:

• Over-the-counter pain medications

In more severe cases:

• Opiates
• Narcotic medications
• Anti-seizure medications

A doctor may prescribe a lidocaine patch or anti-depressants to relieve symptoms.

Patients should thoroughly discuss neuropathy medication with a doctor before proceeding.

Chiropractic/Massage/Physical Therapy

Various manual therapies can benefit symptoms in neuropathy treatment.

A therapist or chiropractor will perform various manipulation techniques, and teach exercises and stretches to help improve symptoms combined with increased muscle strength/control.

A therapist may also recommend braces or splints to improve mobility.

Patients should attend all physical therapy sessions to gain maximum benefits.

Acids

Supplements like:

• Essential acids called ALA (alpha-Lipoic acid)
• GLA (gamma-linolenic acid) and omega-3 fatty acids

These can have a beneficial effect on diabetic peripheral neuropathy.

L-Carnitine

L-carnitine is a substance that the body makes and stores in the:

• Liver
• Brain

There have been reports that certain diabetics with neuropathy symptoms could regain regular sensation in the limbs when they increased their consumption of carnitine called acetyl-L-carnitine.

• Red meat
• Peanut butter
• Dairy products

Are good dietary sources of this nutrient.

Supplements are also available at health food stores and pharmacies and health/wellness clinics.

Vitamin Supplements

Vitamin deficiencies can result in peripheral neuropathy in some people.

Therefore there needs to be a replenishing of vitamins:

• B
• B12
• E

These can help to decrease symptoms.

Recommended dosages are 300mg daily of vitamin E.

Doses of the different B vitamins differ, but one option for patients is to take a daily B-complex supplement.

Herb Supplements

Herbal remedies are an alternative to explore.

St. John's Wort, is a herbal supplement that can be taken orally and can reduce the pain.

Topical creams that have capsaicin, which is an anti-inflammatory found in chili peppers, can reduce the burning sensation.

Acupuncture

Acupuncture can be an effective way to manage peripheral neuropathy.

Acupuncture uses pressure points throughout the body to realign the body's energy, called the qi or chi.

Also, movement therapy is a way to manage the condition.

Tai chi and yoga can help:

• Align the body
• Mind
• Encourage relaxation
• Distract from the pain

El Paso’s Premier Wellness & Injury Care Clinic.

Our services are specialized and focused on injuries and the complete recovery process. Our areas of practice include:

• Wellness & Nutrition
• Chronic Pain
• Personal Injury
• Auto Accident Care
• Work Injuries
• Back Injury
• Low Back Pain
• Neck Pain
• Migraine Treatment
• Sports Injuries
• Severe Sciatica
• Scoliosis
• Complex Herniated Discs
• Fibromyalgia
• Chronic Pain
• Stress Management
• Complex Injuries

As El Paso’s Chiropractic Rehabilitation Clinic & Integrated Medicine Center, we passionately are focused on treating patients after frustrating injuries and chronic pain syndromes.

We focus on improving your ability through flexibility, mobility and agility programs custom-tailored for all age groups and disabilities.

We want you to live a life filled with more energy, a positive attitude, better sleep, less pain, proper body weight and educated on how to maintain this way of life.

We're Ready To Help Get You Healthy!

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When compared to other central nervous system (CNS) health issues, chronic neurodegenerative diseases can be far more complicated. Foremostly, because the compromised mitochondrial function has been demonstrated in many neurodegenerative diseases, the resulting problems in energy sources are not as severe as the energy collapse in ischemic stroke. Therefore, if excitotoxicity contributes to neurodegeneration, a different time of chronic excitotoxicity needs to be assumed. In the following article, we will outline what is known about the pathways that may cause excitotoxicity in neurodegenerative diseases. We will specifically discuss that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies.

Previous research studies suggest that L-aspartate, like L-glutamate, triggers excitatory activity on neurons. L-aspartate functions with L-glutamate in the synaptic vesicles of asymmetric excitatory synapses. But, the total concentration of these in the human brain (0.96-1.62 μmol/gram wet weight), their extracellular concentrations in the cortex as measured by microdialysis (1.62 μM for L-aspartate and 9.06 μM for L-glutamate) and their supply according to immunohistochemistry suggest that L-aspartate is significantly less abundant than L-glutamate. Moreover, L-aspartate is a powerful agonist for NMDA receptors but not for other iGluRs with an EC50 just eight-fold higher than that of L-glutamate. EAATs which play a fundamental role in the uptake of all vesicular released L-glutamate in the central nervous system (CNS) also requires the utilization of L-aspartate. L-aspartate is perhaps as less essential as L-glutamate connected to the total excitatory activity associated with iGluRs. Along with its role as a neurotransmitter, as previously mentioned, L-aspartate is also necessary as a substrate for aspartate amino-transferase which turns into 2-oxoglutarate and L-glutamate to transport to the cortical vesicles of glutamatergic neurons which may also consequently and indirectly increase L-glutamate release.

L-glutamate is one of the main excitatory neurotransmitters in the human brain and it plays an essential role in practically all activities of the nervous system. In the following article, we will discuss the general principles of L-glutamate signaling in the brain. Then, we will demonstrate this scheme by describing the different pools of extracellular glutamate, including the synaptic, the perisynaptic, and the extrasynaptic, resulting from vesicular and non-vesicular sources or abnormally located glutamate receptors outside of synapses as well as discuss their possible physiological functions in the human brain.

Excitotoxicity is a pathological mechanism seen in a variety of health issues where an excessive synaptic excitation causes neuronal death and is also believed to be caused by the extracellular accumulation of the excitatory neurotransmitter glutamate, which triggers and connects ionotropic N-methyl-D-aspartate glutamatergic receptors (NMDARs) in the brain. Generally, NMDARs regulate and maintain calcium in cells to help manage physiological mechanisms like synaptic plasticity and memory, however, excessive stimulation can ultimately increase intracellular calcium which triggers cell death signaling to activate apoptosis. This pathological mechanism has been suggested in a variety of health issues, such as traumatic brain injury (TBI) and Alzheimer’s disease (AD), where it is extensively examined to understand health issues and treatment approaches. In a stroke, excitotoxicity has been shown to be the main pathological mechanism where neuronal damage happens and it is considered to be a well-known goal for many recent attempts at developing stroke therapeutics.

Stroke is an acute brain health issue which causes neuronal damage which has currently no safe and effective neuroprotective treatment approaches. Immediately following a stroke, the brain tissue loses blood perfusion and the center of the infarct deteriorates quickly. This then causes milder ischemia and many brain cells or neurons will result in delayed death which can take up to several hours or even days. Research studies show that the mechanism of cell death is mainly NMDA receptor-dependent excitotoxicity. In ischemic areas, extracellular glutamate levels increase while preventing glutamate release, synaptic activity, or NMDAR activation which was capable of limiting cell death in a variety of stroke models. Thus, preventing excitotoxicity is an important treatment approach for reducing brain damage and improving patient outcome measures following a stroke, and this has definitely encouraged extensive efforts towards developing NMDA receptor-based stroke treatment approaches over the last two decades. Unfortunately, these have largely met with rather disappointing results. Several research studies have failed to find the expected efficiency of NMDAR for decreasing brain injuries. The reasons behind the basic research study results and clinical trials are still unknown, however, several reasons have been suggested. These include, but are not limited to, the inability to utilize the correct doses necessary for neuroprotection due to their side-effects, the inability to use the drugs within their neuroprotective windows, poor experimental designs, and heterogeneity in the patient population. However, as we will briefly summarize in the following article, improvement in our understanding of the physiological and pathological mechanisms of NMDAR activation as well as the different pathways connected to different NMDAR subtypes, has allowed researchers to develop new treatment approaches which improve therapeutic windows and increase specificity for death signaling pathways, achieving neuroprotection without interrupting other essential signaling pathways downstream of the NMDAR receptor.

Many healthcare professionals believe that peripheral neuropathy, which affects the peripheral nerves or the nerves which connect from the brain and spinal cord to the upper and lower extremities, can be permanent or irreversible. However, healthcare professionals like Dr. John Coppola and Dr. Valerie Monteiro have demonstrated that peripheral neuropathy can be treated through the utilization of a variety of treatment methods and techniques.

Dr. Coppola and Dr. Monteiro describe that because peripheral neuropathy can manifest due to a variety of health issues, such as diabetes, treating the underlying cause of a patient's peripheral neuropathy can help treat their symptoms. The 5 critical keys for defeating peripheral neuropathy are ultimately described to help promote overall health and wellness. Dr. Alex Jimenez, a chiropractor in El Paso, Tx, can help ease symptoms associated with peripheral neuropathy. Dr. Alex Jimenez is the non-surgical choice for peripheral neuropathy.

Peripheral Neuropathy Relief & Treatment | El Paso, TX (2019)

Neuropathy is a medical term used to describe a collection of general diseases or malfunctions which affect the nerves. The causes of neuropathy, or nerve damage, can vary greatly among each individual and these may be caused by a number of different diseases, injuries, infections, and even vitamin deficiency states. However, neuropathy can most commonly affect the nerves that control the motor and sensory nerves. Because the human body is composed of many different kinds of nerves which perform different functions, nerve damage is classified into several types.

Neuropathy can also be classified according to the location of the nerves being affected and according to the disease-causing it. For instance, neuropathy caused by diabetes is called diabetic neuropathy. Furthermore, depending on which nerves are affected will depend on the symptoms that will manifest as a result. Below we will discuss several specific types of neuropathies clinically treated by chiropractors, physical therapists and physical medicine doctors alike, as well as briefly describing their causes and their symptoms.

Peripheral neuropathy, which is often simply referred to as “neuropathy,” is a state that happens when your nerves become damaged or injured, oftentimes simply disrupted. It’s estimated that neuropathy affects roughly 2.4 percent of the general populace and approximately 8 percent of people older than age 55. However, this quote doesn’t include people affected by neuropathy caused by physical trauma to the nerves.

Types

Neuropathy can affect any of the three types of peripheral nerves:

• Sensory nerves, which transmit messages from the sensory organs, eyes, nose to the brain
• Motor nerves, which track the conscious movement of the muscles
• Autonomic nerves, which regulate the involuntary functions of the body

Sometimes, neuropathy will only impact one nerve. This is medically referred to as mononeuropathy and instances of it include:

• Ulnar neuropathy, which affects the elbow
• Radial neuropathy, which affects the arms
• Peroneal neuropathy, which affects the knees
• Femoral neuropathy, which affects the thighs
• Cervical neuropathy, which affects the neck

Sometimes, two or more isolated nerves in separate regions of the body can become damaged, injured or disrupted, resulting in mono neuritis multiplex neuropathy. Most often, however, multiple peripheral nerves malfunction at the same time, a condition called polyneuropathy. According to the National Institute for Neurological Disorders and Stroke, or the NINDS, there are over 100 kinds of peripheral neuropathies.

Causes

Neuropathies are often inherited from birth or they develop later in life. The most frequent inherited neuropathy is the neurological disease Charcot-Marie-Tooth disease, which affects 1 in 2,500 people in the USA. Although healthcare professionals are sometimes not able to pinpoint the exact reason for an acquired neuropathy, medically referred to as idiopathic neuropathy, there are many known causes for them, including systemic diseases, physical trauma, infectious diseases, and autoimmune disorders.

A systemic disease is one which affects the whole body. The most frequent systemic cause behind peripheral neuropathy is diabetes, which can lead to chronically high blood glucose levels that harm nerves.

Other systemic issues can cause neuropathy, including:

• Kidney disorders, which permit high levels of nerve-damaging toxic chemicals to flow in the blood
• Toxins from exposure to heavy metals, including arsenic, lead, mercury, and thallium
• Certain drugs and/or medications, including anti-cancer medications, anticonvulsants, antivirals, and antibiotics
• Chemical imbalances because of liver ailments
• Hormonal diseases, including hyperthyroidism, which disturbs metabolic processes, potentially inducing cells and body parts to exert pressure on the nerves
• Deficiencies in vitamins, such as E, B1 (thiamine), B6 (pyridoxine), B12, and niacin, that can be vital for healthy nerves
• Alcohol abuse, which induces vitamin deficiencies and might also directly harm nerves
• Cancers and tumors that exert damaging pressure on nerve fibers and pathways
• Chronic inflammation, which can damage protective tissues around nerves, which makes them more vulnerable to compression or vulnerable to getting inflamed and swollen
• Blood diseases and blood vessel damage, which may damage or injure nerve tissue by decreasing the available oxygen supply

Signs and Symptoms

Depending on the reason and unique to each patient, signs, and symptoms of neuropathy can include:

• Pain
• Tingling
• Burning/prickling sensations
• Increased sensitivity to touch
• Muscle weakness
• Temporary or permanent numbness;
• Paralysis
• Dysfunction in glands or organs
• Impairment in urination and
• Sexual function

Such signs and symptoms are dependent on whether autonomic, sensory, or motor nerves, as well as a combination of them, are ultimately affected. Autonomic nerve damage can influence physiological functions like blood pressure or create gastrointestinal problems and issues. Damage or dysfunction in the sensory nerves may impact sensations and sense of equilibrium or balance, while harm to motor nerves may affect movement and reflexes. When both sensory and motor nerves are involved, the condition is known as sensorimotor polyneuropathy.

Complications

Peripheral neuropathy may result in several complications, as a result of disease or its symptoms. Numbness from the ailment can allow you to be less vulnerable to temperatures and pain, making you more likely to suffer from burns and serious wounds. The lack of sensations in the feet, for instance, can make you more prone to developing infections from minor traumatic accidents, particularly for diabetics, who heal more slowly than other people, including foot ulcers and gangrene.

Furthermore, muscle atrophy may cause you to develop particular physical disfigurements, such as pes cavus, a condition marked by an abnormally high foot arch, and claw-like deformities in the feet and palms.

Neuropathy Treatment

The first step in neuropathy treatment should be finding the root cause that's causing the neuropathy.

Treatment of diseases such as:

• Diabetes
• Guillain-Barre syndrome
• Rheumatoid arthritis
• Sarcoidosis
• Other underlying diseases

Prevents continued nerve damage and in some cases heals the damaged nerves.

If you are unaware of any underlying disease that is causing the peripheral neuropathy, make sure to let your doctor know of abnormal symptoms you may be experiencing. 

Medication

Peripheral neuropathy can be treated with various medications.

The first type used to treat mild symptoms are:

• Over-the-counter pain medications

In more severe cases:

• Opiates
• Narcotic medications
• Anti-seizure medications

A doctor may prescribe a lidocaine patch or anti-depressants, as well to relieve symptoms.

Patients should thoroughly discuss medication for neuropathy treatment with a doctor before proceeding.

Physical Therapy

Physical therapy can benefit symptoms in neuropathy treatment.

A therapist will teach the patient exercises and stretches to help improve symptoms and increase muscle strength/control.

A therapist may also recommend braces or splints to improve mobility.

Patient's should attend all physical therapy sessions to gain the maximum benefits. 

Acids

Supplements like:

• Essential acids called ALA (alpha-Lipoic acid)
• GLA (gamma-linolenic acid) and omega-3 fatty acids

These can have a beneficial effect on diabetic peripheral neuropathy.

L-Carnitine

L-carnitine is a substance that the body makes and stores in the:

• Liver
• Brain

There have been reports that certain diabetics with neuropathy symptoms could regain regular sensation in the limbs when they increased their consumption of carnitine called acetyl-L-carnitine.

• Red meat
• Peanut butter
• Dairy products

Are good dietary sources of this nutrient.

Supplements are also available at health food stores and pharmacies and health/wellness clinics. 

Vitamins/Minerals

Vitamin deficiencies can result in peripheral neuropathy in some people.

Therefore there needs to be a replenishing of vitamins:

• B
• B12
• E

Can help to decrease symptoms.

Recommended dosages are 300mg daily of vitamin E.

Doses of the different B vitamins differ, but one option for patients is to take a daily B-complex supplement.

Herbal Supplements

Herbal remedies are an alternative to explore.

St. John's Wort, is a herbal supplement that can be taken orally and can reduce the pain.

Topical creams that have capsaicin, which is an anti-inflammatory found in chili peppers, can reduce the burning sensation.

Traditional Chinese Medicine TCM

Acupuncture can be an effective way to manage peripheral neuropathy.

Acupuncture uses pressure points throughout the body to realign the body's energy, called the qi or chi.

Also, movement therapy is a way to manage the condition.

Tai chi and yoga can also help:

• Align the body
• Mind
• Encourage relaxation
• Distract from the pain

Even if the neuropathy treatment is only temporary, it can still help.

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Traumatic brain injury (TBI) is one of the most common causes of disability and death among the general population, especially in young adults. Additionally, TBI is associated with a variety of neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). It is essential for patients and healthcare professionals to understand the pathophysiological mechanisms of traumatic brain injury and neurodegenerative diseases to diagnose factors which may ultimately cause neurodegeneration associated with TBI as well as determine possible treatment approaches.

Oxidative stress, neuroinflammation, and glutamatergic excitotoxicity have previously been associated with TBI and neurodegenerative diseases. As a matter of fact, oxidative stress is believed to be an essential pathological mechanism which connects TBI to neurodegenerative diseases. Research studies have demonstrated that reactive oxygen species and their subsequent byproducts may play a role as novel fluid markers for the identification and monitoring of cellular damage. These reactive oxygen species can also serve as a suitable treatment approach to ultimately help reduce the risk of neurodegenerative diseases and promote quality of life for people suffering from TBI and other health issues.

Traumatic brain injury (TBI) is one of the most common causes of disability and death in people. About 1.6 million individuals suffer traumatic brain injuries in the United States every year. TBI can cause a process of injury which may ultimately cause a variety of neurodegenerative diseases and other health issues. Many of the neurodegenerative diseases following TBI include health issues such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS).

The mechanisms underlying the pathogenesis which result in these type of neurodegenerative diseases, however, are still completely misunderstood. Where many of the health issues following TBI have a high incidence, there are currently only several treatment approaches which can help prevent the pathological development of chronic neurological diseases.

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